Abstract
Inflammatory bowel disease (IBD) is a chronic inflammatory disorder of the gastrointestinal tract resulting from the homeostasis imbalance of intestinal microenvironment, immune dysfunction, environmental and genetic factors, and so on. This disease is associated with multiple immune cells including regulatory T cells (Tregs). Tregs are a subset of T cells regulating the function of various immune cells to induce immune tolerance and maintain intestinal immune homeostasis. Tregs are correlated with the initiation and progression of IBD; therefore, strategies that affect the differentiation and function of Tregs may be promising for the prevention of IBD-associated pathology. It is worth noting that tryptophan (Trp) metabolism is effective in inducing the differentiation of Tregs through microbiota-mediated degradation and kynurenine pathway (KP), which is important for maintaining the function of Tregs. Interestingly, patients with IBD show Trp metabolism disorder in the pathological process, including changes in the concentrations of Trp and its metabolites and alteration in the activities of related catalytic enzymes. Thus, manipulation of Treg differentiation through Trp metabolism may provide a potential target for prevention of IBD. The purpose of this review is to highlight the relationship between Trp metabolism and Treg differentiation and the role of this interaction in the pathogenesis of IBD.
Highlights
Inflammatory bowel disease (IBD) is an autoimmune disease with high incidence and unclear etiology, mainly including ulcerative colitis (UC), Crohn’s disease (CD), and indeterminate colitis (IC) [1]
Tregs are associated with the development of IBD and strategies to manipulate Treg differentiation by Trp metabolism may lead to new therapeutic approaches for the treatment of IBD (Figure 4)
It is important for researchers to elucidate the exact regulatory mechanism of Trp metabolism in Tregs during the development of IBD
Summary
Inflammatory bowel disease (IBD) is an autoimmune disease with high incidence and unclear etiology, mainly including ulcerative colitis (UC), Crohn’s disease (CD), and indeterminate colitis (IC) [1]. The generation, differentiation, and function of Tregs are significantly affected by the availability of amino acids in the local microenvironment. Mediators of Inflammation intestinal tract, Trp undergoes several different metabolic pathways, and Trp metabolism can influence the differentiation and function of Tregs. Trp starvation and Trp catabolites could induce the generation of a regulatory phenotype in naive CD4+ T cells, and previous studies indicated that there is a close relationship between indoleamine 2,3-dioxygenase (IDO) activity and the occurrence of Tregs [12,13,14]. Regulation of Tregs through altering Trp metabolism may provide potential targets for prevention of IBD. We provide an in-depth review highlighting the understanding of the regulatory roles of Trp metabolism in Treg differentiation and discuss the availability of manipulating Trp metabolism to Tregs, which further prevent or ameliorate IBD
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
